When functioning properly, the human heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout the body's circulatory system. However, some people have irregular cardiac rhythms, referred to as cardiac arrhythmias. Such arrhythmias result in diminished blood circulation. One mode of treating cardiac arrhythmias uses drug therapy. Drugs are often effective at restoring normal heart rhythms. However, drug therapy is not always effective for treating arrhythmias of certain patients. For such patients, an alternative mode of treatment is needed. One such alternative mode of treatment includes the use of a cardiac rhythm management system. Such systems are often implanted in the patient and deliver therapy to the heart.
Cardiac rhythm management systems include, among other things, pacemakers, also referred to as pacers. Pacers deliver timed sequences of low energy electrical stimuli, called pace pulses, to the heart, such as via an intravascular leadwire or catheter (referred to as a “lead”) having one or more electrodes disposed in or about the heart. Heart contractions are initiated in response to such pace pulses (this is referred to as “capturing” the heart). By properly timing the delivery of pace pulses, the heart can be induced to contract in proper rhythm, greatly improving its efficiency as a pump. Pacers are often used to treat patients with bradyarrhythmias, that is, hearts that beat too slowly, or irregularly. Some pacers coordinate atrial and ventricular contractions to improve pumping efficiency. Cardiac rhythm management systems also include coordination devices for coordinating the contractions of both the right and left sides of the heart for improved pumping efficiency.
Cardiac rhythm management systems also include defibrillators that are capable of delivering higher energy electrical stimuli to the heart. Such defibrillators also include cardioverters, which synchronize the delivery of such stimuli to sensed intrinsic heart depolarizations. Defibrillators are often used to treat patients with tachyarrhythmias, that is, hearts that beat too quickly. Such too-fast heart rhythms also cause diminished blood circulation because the heart isn't allowed sufficient time to fill with blood before contracting to expel the blood. Such pumping by the heart is inefficient. A defibrillator is capable of delivering a high energy electrical stimulus that is sometimes referred to as a defibrillation countershock, also referred to simply as a “shock.” The countershock interrupts the tachyarrhythmia, allowing the heart to reestablish a normal rhythm for the efficient pumping of blood. In addition to pacers, cardiac rhythm management systems also include, among other things, pacer/defibrillators that combine the functions of pacers and defibrillators, drug delivery devices, and any other implantable or external systems or devices for diagnosing or treating cardiac arrhythmias.
One problem faced by cardiac rhythm management systems is the proper timing relationship between a sensed or paced atrial depolarization and the subsequent delivery during the same cardiac cycle of a ventricular pacing pulse. This atrioventricular time interval is referred to as the A-V delay. The A-V delay provided by a cardiac rhythm management system may be programmed by the physician to tailor the therapy for a particular patient. The actual value of the A-V delay affects the blood flow from the atrium to the ventricle and, therefore, affects the cardiac output of the heart. The blood flow from the atrium to the ventricle has two components. After the ventricle has completed a contraction, it begins to relax, with blood entering the ventricle from the corresponding atrium when the atrial pressure exceeds the ventricular pressure. This pulse-like fluid flow is sometimes referred to as the “E-wave” of a Doppler echocardiograph. Next, the atrium contracts to actively expel a second pulse-like flow of fluid, sometimes referred to as the Doppler echocardiographic “A-wave,” to the ventricle. For a given fixed time interval between ventricular contractions, if the A-V delay is set too long, then the atrial contraction is moved closer to the preceding ventricular contraction. Because the A-wave and the E-wave occur closer together in time, there is a reduction in total ventricular filling time. By contrast, if the A-V delay is set too short, then the ventricle does not receive the full benefit of the blood flow during the A-wave. For these and other reasons, there is a need to select an A-V delay value that promotes increased blood flow from the atrium to the ventricle, thereby increasing cardiac output.